| 研究実績の概要 |
Chemical Splicing inhibition leads to an increase in cellular heterochromatin content. This increase depends on the small RNA processing machinery. We confirmed this increase in heterochromatin by chromatin immunoprecipitation and and high throughput sequencing. In presence of the small molecule inhibitor Spliceostatin A (SSA) a significant increase in histone methylation levels was observed in specific locations. We had hypothesized that small RNAs would map to heterochromatin loci on the chromosome. Thus far we have not been able to confirm this hypothesis as data analysis proved more challenging than anticipated, as experimental data proved noisier than we had hoped. We are currently in the process of refining our data analysis and partially resequencing of samples to obtain a more comprehensive view of the cell's heterochromatin landscape. We have added additional time points to our analysis and are using different mapping strategies to make most of the obtained data. Using small RNA interference we are further in the process of identifying protein factors responsible to changes in heterochromatinization under chemical splicing inhibition. A re-evaluation of small RNA contribution is under way.
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